Evidence map›Paper›PMID 20119957›Full record

ArticleElectrophoresis2010

Differential expression of proteins in fetal brains of alcohol-treated prenatally C57BL/6 mice: a proteomic investigation.

Youssef Sari, Min Zhang, Yehia Mechref

Abstract read
In one paragraph

Article in Electrophoresis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.5field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Fetal regional brain protein signature in FASD rat model.Reproductive toxicology (Elmsford, N.Y.) · 2018
    Article
  6. Article
  7. Proteomic approaches and identification of novel therapeutic targets for alcoholism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Prohibitin reduces mitochondrial free radical production and protects brain cells from different injury modalities.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Youssef SariNeuroscience Program, Department of Psychological and Brain Sciences, Indiana University Bloomington, IN 47405, USA. ysari@indiana.edu
Min Zhang
Yehia Mechref
Indiana University Bloomington · USPurdue University West Lafayette · US

Funding

Molecular mechanism of ADNF and ADNP peptides in prevention of mitochondrial dysfR21AA017735 · NIAAA · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI SARI, YOUSSEF · 2009 to 2010
$403k
Molecular mechanism of ADNF and ADNP peptides in neuroprotection to alcoholR21AA016115 · NIAAA · TRUSTEES OF INDIANA UNIVERSITY · PI SARI, YOUSSEF · 2007 to 2008
$360k
NIAAA NIH HHS R21AA016115NIAAA NIH HHS R21 AA017735NIAAA NIH HHS R21AA017735
6 · The paper itself

Abstract

Alcohol is known to impede the growth of the central nervous system and to induce neurodegeneration through cellular apoptosis. We have previously shown that moderate prenatal alcohol exposure results in brain defects at different stages of development. In this study, we further characterize the proteomic architecture underlying ethanol teratogenesis during early fetal brain development using chromatography in conjunction with a LC-MS/MS system. Pregnant C57BL/6 mice were exposed from embryonic day 7 (E7) to E13 with either a 25% ethanol derived calorie or pair-fed liquid diets. At E13, fetal brains were collected from five dams for each group. Individual brains were homogenized and the extracted proteins were then tryptically digested and analyzed by LC-MS/MS. Label-free quantitative proteomic analyses were performed on proteomes extracted from fetal brains of both alcohol-treated (ALC) and pair-fed groups. These analyses demonstrated that prenatal alcohol exposure induced significant downregulation (p<0.001) of the expression of mitochondrial enzymes including ADP/ATP translocase 1, ATP synthase subunit alpha and ubiquinol-cytochrome-c reductases. In addition, mitochondrial carrier homolog 1, which plays a role in apoptosis, was significantly downregulated (p<0.001) in the ALC group. Moreover, among the cytosolic proteins that were significantly downregulated (p<0.001) are Bcl-2, 14-3-3 protein and calmodulin. Significant downregulation (p<0.001) of proteins that are critical for fetal brain development was observed such as prohibitin and neuronal migration protein doublecortin. These findings provide information about possible mechanisms underlying the effects of prenatal alcohol exposure during early embryonic stage.

Indexed as

Maternal ExposureProteomicsAbnormalities, Drug-InducedAnimalsBrainChromatography, LiquidCytosolEmbryonic DevelopmentEthanolFemaleGene Expression Regulation, DevelopmentalMass SpectrometryMiceMice, Inbred C57BLMitochondriaPregnancyEthanolProteinsTeratogens

Identifiers

PMID20119957
PMCPMC3431165
OpenAlexW2098928648

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.